As a library, NLM provides access to scientific literature.

Inclusion in an NLM
database does not imply endorsement of, or agreement with, the contents by NLM
or the National Institutes of Health.
Learn more: PMC Disclaimer | PMC Copyright Notice

Acad Pathol. 2022; 9(1): 100017. PMCID: PMC9234233

Published online 2022 Jun 21. doi: 10.1016/j.acpath.2022.100017 PMID: 35770199

Educational case: Brain abscess

Rick Bowens, BS∗ and Larry Nichols, MD

The following fictional case is intended as a learning tool within the Pathology
Competencies for Medical Education (PCME), a set of national standards for
teaching pathology. These are divided into three basic competencies: Disease
Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and
Therapeutic Pathology. For additional information, and a full list of learning
objectives for all three competencies, see
https://www.journals.elsevier.com/academic-pathology/news/pathology-
competencies-for-medical-education-pcme.1

Primary objective

Objective NSC2.1: Infections of the CNS. Compare and contrast the clinical, gross, and
microscopic manifestations of common bacterial, viral, and fungal infections of the central
nervous system.

Competency 2: Organ system pathology; Topic: nervous system: Central nervous system
(NSC); Learning goal 2: Infection
Secondary objective

Objective M1.3: Identification. Give examples of the types of testing, and their optimal
usage, performed in microbiology to identify an infectious disease.

Competency 3: Diagnostic medicine and therapeutic pathology; Topic: Microbiology (M);

Learning goal 1: Pathogenesis, diagnosis, and treatment of infectious disease

Patient presentation

A 22-year-old woman presents to a community hospital after having a generalized seizure at

work, which lasted for 5 min and was associated with incontinence of urine. She has an
unremarkable past medical history and denies using alcohol, tobacco or illicit drugs. She
works as a nursing assistant in a nursing home. She is married and lives with her husband
and four young children.

Diagnostic findings, Part 1

At the hospital, the patient’s temperature is 98.4 °F, pulse 134 beats per min, blood pressure
131/70 mmHg and respirations 28 per min. On examination, she is drowsy, staring blankly,
unresponsive to verbal stimuli but without focal neurological findings. Ten minutes after her
arrival, she has a second seizure characterized by unresponsiveness, rigid extremities, head
turned to the side and cyanosis.

Questions/discussion points, Part 1

What are the most common causes of new onset seizures?

The most common causes of seizures vary greatly by age group.2 Fever is the most common
cause of seizures in children. Between 2% and 5% of children have febrile seizures.3
Cerebrovascular disease is the most common cause of seizures in adults over 35 years of
age.2 In young adults such as this patient, the new onset of seizures does not have a single
predominant cause. Trauma is the most common cause, but tumor is a close second most
common cause.2 Gliomas and meningiomas often present with seizures. Drugs, especially
alcohol withdrawal, are an important cause of seizures in young adults. Autoimmune
encephalitis, including anti-NMDR encephalitis in young women with ovarian teratomas, can
present with seizures.4 Infections, including herpes simplex virus encephalitis or
neurocysticercosis, can present with seizures. The cause of new onset seizures is idiopathic
in many young adults.2
The most common causes of recurrent seizures unprovoked by fever or drug toxicity
(epilepsy) also varies by age. Recurrent seizures in a neonate, within 48 h of a difficult birth,
are usually due to severe anoxic brain injury.2 Recurrent unprovoked seizures in an infant are
often due to congenital malformations, for example, cortical plate malformations such as
focal cortical dysplasia, which can exist alone or in association with hippocampal sclerosis or
an adjacent lesion (e.g., glial or glioneuronal tumor, vascular malformation, etc.). Epilepsy
beginning in early childhood may be benign, without intellectual impairment, and may cease
in adolescence. The most common causes of recurrent unprovoked seizures in later childhood
and adolescence shade into those in young adults and include arteriovenous malformations.2

The new onset of seizures can be due to underlying treatable disease, making recognition of
the cause important. Hyponatremia, hypernatremia, hyperglycemia, hypoglycemia,
hypocalcemia, uremia, and thyrotoxicosis are among the many metabolic derangements that
can cause seizures, which resolve with successful treatment of the underlying medical
disease.2 Seizures can be an adverse effect of medications such as cefepime, imipenem,
linezolid, tramadol, bupropion, and many others.2 Illicit drugs such as methamphetamine,
cocaine or high-potency synthetic cannabinoids can cause seizures. Bacterial meningitis can
cause seizures, which will be associated with fever, headache and stiff neck. In immuno-
compromised patients, central nervous system primary lymphoma or opportunistic infections
such as toxoplasmosis can present with the new onset of seizures.2 The most likely cause of
new onset seizures in each patient depends on their age, immunological status, and other
conditions.

Diagnostic findings, Part 2

The patient’s white blood cell count is 11,900/cu mm (70.6% granulocytes, 22.6%
lymphocytes, 6.8% monocytes), hemoglobin 13.1 g/dL, platelets 192,000/cu mm, sodium
138 mEq/L, potassium 3.8 mEq/L, chloride 104 mEq/L, carbon dioxide 19 mEq/L, blood
urea nitrogen 7 mg/dL, creatinine 0.8 mg/dL and glucose 106 mg/dL. Following her second
seizure, the patient’s pulse increases to 145 per min. She is given supplemental oxygen and a
loading dose of phenytoin. Computerized tomography (CT) of the head shows a single 1.5
cm ring-enhancing lesion in the high left parietal lobe with less density in the center of the
lesion and moderate surrounding edema.

Questions/discussion points, Part 2

What is the differential diagnosis for a ring-enhancing lesion in the brain?

The most common causes of a ring-enhancing lesion in the brain can be sorted into five
groups: metastases, abscesses, glioblastomas, infarcts (or inflammation) and contusions.5
Taking the first letter of each, the acronym MAGIC can serve as a memory aide for the most
common causes of a ring-enhancing lesion. The acronym is only a starting point.
Glioblastomas are only one type of the high grade brain primary tumors that can cause a
ring-enhancing lesion. A little clarification of the letter “I” conditions is needed because only
infarcts in the subacute phase are likely to produce a ring-enhancing lesion, and multiple
inflammatory conditions can cause ring-enhancing lesions. Cysticercosis, toxoplasmosis and
tuberculosis are typically associated with ring-enhancing lesions, but demyelinating diseases
can also sometimes produce lesions that are ring-enhancing. Metastases are perhaps the most
common etiology of a ring-enhancing lesion in the United States, where the annual incidence
of tumors in the brain is 46 per 100,000, but only one-third of these are primary brain
tumors.6 Brain metastases and glioblastomas are usually seen in older adults. Brain abscesses
are far less common, with reported annual incidence ranging from 0.4 to 0.9 per 100,000.7
Cerebral infarcts are primarily in older adults with advanced atherosclerotic cardiovascular
disease and rarely first detected in a subacute phase associated with a ring-enhancing lesion.
The most likely cause of a ring-enhancing lesion depends on the age of the patient. One
approach to the differential diagnosis is to first try to put the lesion into one of two broad
categories of inflammatory diseases or non-inflammatory diseases. If inflammatory, the next
step is to try to put the lesion into the subcategory of infectious diseases or non-infectious
diseases. The correct diagnosis is most likely to come from an interdisciplinary collaborative
teamwork of radiologists and clinicians.

Diagnostic findings, Part 3

The patient is transferred to a large public hospital, where she is alert, oriented and without
focal neurological findings. Her temperature is 97.8 °F, pulse 80 beats/minute, blood pressure
94/64 mmHg and respirations 18 per min. On review of systems, the patient reports having a
headache for the previous 3 days. She also reports visiting an emergency room for a severe
headache 3 years prior. She denies having any severe headaches since that time. The scan
from the other hospital is reviewed by a radiologist at the public hospital and diagnosed as
abscess, cysticercosis or tumor. The prevalent causes of brain lesions in young adult patients
in this hospital are abscesses from endocarditis in intravenous drug users and cysticercosis in
recent immigrants. The medical team caring for the patient judges abscess unlikely, and their
diagnosis is “rule out glioma." The patient is treated with oral phenytoin and dexamethasone,
but no other medications. She is clinically stable, without further seizures.

On hospital day 2, the patient's white blood cell count is 14,300/cu mm (66% segmented
neutrophils, 1% bands), hemoglobin 12.2 g/dL, platelets 204,000/cu mm, calcium 8.9 mg/dL,
phosphorus 3.7 mg/dL, glucose 97 mg/dL, bilirubin 0.5 mg/dL, alkaline phosphatase 85 U/L,
alanine aminotransferase 21 U/L, aspartate aminotransferase 20 U/L, globulin 7 g/dL,
albumin 3.9 g/dL, lactate dehydrogenase 129 U/L and creatine phosphokinase 57 U/L.
Testing for human immunodeficiency virus infection is negative. On day 3, magnetic
resonance imaging (MRI) scan with gadolinium shows a bilobed ring-enhancing lesion with
a thick irregular wall in the left parietal lobe, measuring 2.1× 1.5 × 1.5 cm, with moderate
surrounding edema; there is also mild mucosal thickening in the right frontal sinus. The
radiologist's diagnosis is: "suspicious for a primary brain tumor." With this presumptive
diagnosis, the patient is scheduled for a non-emergency brain biopsy two weeks later. She is
clinically stable and discharged home to await her brain biopsy.

Questions/discussion points, Part 3

How does this additional clinical information alter the differential diagnosis?

The patient has a mild and increasing leukocytosis, which suggests the possibility of
infection, but also could represent a nonspecific stress response. She has tachycardia without
fever, which would fit with a stress response. She has no heart murmur to suggest a cardiac
source of emboli to the brain. Some brain abscesses are associated with simultaneous liver
abscesses, so the normal liver tests are helpful in making brain abscess less likely. The
apparent increase in size of the brain lesion in this case from 1.5 cm on CT to 2.1 cm on MRI
a few days later is not interpreted as true growth or progression, but presumably attributed to
the differences between the types of scan or the slices scanned. The lesions of
neurocysticercosis are often multiple and often calcified, making that less likely in this case.
Inflammatory brain lesions and tumors may have a similar pattern of ring enhancement
around a non-enhancing core of cystic components or necrosis.8 Glioblastoma tends to be
more spherical than brain abscess, which can help differentiating these conditions.9 Texture
analysis of ring-enhancing lesions on MRI based on machine learning approaches are
computer-aided diagnostic tools that can assist radiologists in differentiating inflammatory
brain lesions from tumors.8

Diagnostic findings, Part 4

The patient is re-admitted to the hospital one week later with aphasia and word-finding
difficulty. On examination, she also has mild right pronator drift. The patient's white blood
cell count is 16,500/cu mm (86% segmented neutrophils, 4% bands), hemoglobin 14.1 g/dl,
platelets 327,000/cu mm, glucose 137 mg/dL and lactate dehydrogenase 213 U/L. She is
continued on oral phenytoin and dexamethasone therapy. She is clinically stable. She
undergoes her previously scheduled stereotactic brain biopsy. The biopsy is evaluated in the
frozen section room at the time of surgery and shows findings such as those in Fig. 1. Normal
brain for comparison is shown in Fig. 2.
 Fig. 1

Gliosis with loss of neurons and increased numbers of glial cells (H&E, X40).

Fig. 2

Normal brain for comparison, with neurons (one indicated by thin arrow), some associated with glial
cells (one indicated by thick arrow) (H&E, X40).

The pathologist sees the abundant glial cells and knows the diagnoses made by the
radiologist and the clinicians. She recognizes that the findings could represent a glioma, but
knows they could also represent reactive gliosis in the ring-enhancing margin of the lesion
and that a sample from the less dense center of the lesion might be more specifically
diagnostic. She asks the neurosurgeon to make another pass, deeper into the lesion, and get
another biopsy. This second biopsy shows findings such as those in Fig. 3.

Fig. 3

Necrotic brain tissue with numerous neutrophils recognizable by their multilobed nuclei (H&E, X40).

Recognizing the necrotic brain tissue infiltrated by large numbers of neutrophils as an

abscess, the pathologist instructs the neurosurgeon what appropriate samples to take for the
clinical microbiology laboratory and what tests to order on them.

Questions/discussion Points 4

What pathogens cause brain abscesses?

Brain abscesses can be caused by bacteria (aerobic or anaerobic), fungi, mycobacteria, or
parasites (helminths or protozoa).7 Most brain abscesses are due to bacteria, often from the
normal oral flora, and many brain abscesses are polymicrobial, including both aerobes and
anaerobes.10,11 The organisms most commonly isolated are anaerobic bacteria, aerobic and
microaerophilic streptococci, various Enterobacteriaceae, and Staphylococcus aureus.10
Streptococcus intermedius has emerged as a frequent pathogen in brain abscesses.12,13
Among the anaerobes, Fusobacterium nucleatum is frequently a pathogen in brain
abscesses.14,15 Actinomyces species are sometimes among the anaerobic pathogens in
polymicrobial brain abscesses.16,17 Mycobacterium tuberculosis can cause a brain mass with
necrosis.18 Nocardia species are an important cause of brain abscess in
immunocompromised patients.19 Fungi such as Aspergillus species can also cause brain
lesions with necrosis in immunocompromised patients.20

What are appropriate samples for the clinical microbiology laboratory to identify the
pathogens in a brain abscess?

Aspirate of the liquid center of a brain abscess is usually the best sample for the clinical
microbiology laboratory to identify the pathogens causing the infection. Cerebrospinal fluid
or blood cultures identify a pathogen in approximately 25% of cases, particularly in patients
with meningitis, but the risk of brain herniation must be taken into account and lumbar
puncture should be performed only when there is clinical suspicion of meningitis or abscess
rupture into the ventricular system and there are no contraindications for lumbar puncture.7
Gram stain, aerobic and anaerobic cultures are generally the most essential testing. In
immuno-compromised patients, smears and cultures should also be done for mycobacteria,
nocardia species, and fungi; nucleic acid molecular testing by polymerase-chain-reaction
(PCR) assay for Toxoplasma gondii should be performed as well.7 If a bacterial etiology is
strongly suspected but bacterial cultures are negative, PCR-based 16S ribosomal DNA
sequencing may provide a definitive diagnosis, enabling targeted antimicrobial therapy. If
available and resources allow it, molecular testing can be particularly helpful in identifying
anaerobic pathogens in brain abscesses.21 Molecular diagnostic methods are continuously
evolving and next generation sequencing may reveal multiple pathogens as well as expanding
the spectrum of pathogens detected.22 The best specimen for such testing may be frozen and
the need for it not evident at the time of collection, so it could be helpful for the pathologist
to suggest freezing some of the material collected for possible future use.

What is the pathological evolution of a brain abscess?

Intraparenchymal brain abscess starts with spread from a contiguous site of infection in about
half of cases.7 Such contiguous foci include the paranasal sinuses, the nose, mastoid air cells,
the ears, the teeth, and sites of trauma or invasive neurosurgical procedures.23 Brain abscess
starts from hematogenous spread of infection in about one third of cases, and from unknown
7
mechanisms in the remaining non-contiguous non-hematogenous cases.7 Hematogenous
brain abscess is often secondary to septic emboli from infective endocarditis. Cerebral
abscess evolution can be described in 4 stages: early cerebritis, late cerebritis, early capsule
formation, and late capsule formation.24 Ring enhancement represents the granulation tissue
of evolving capsule in the later phases of the host response to contain the infection. The
characteristic MRI feature of mature necrotizing brain abscess is fluid hyperintense relative
to CSF and hypointense relative to white matter on T1-weighted imaging. T2-weighted
imaging showing hyperintensity compared to both CSF and gray matter.24 The gross and
microscopic pathology of brain abscesses do not vary enough with specific pathogens to
allow for helpful comparison and contrast.

What are the clinical manifestations of a brain abscess?

The signs and symptoms of a brain abscess are nonspecific, variable and rarely point to a
specific pathogen. The reported percentages of various clinical manifestations have a broad
range and some are lumped into categories that vary among the reports. As shown in Table 1,
the most common presenting symptom is headache, typically generalized.7,11,23,25 Focal
neurological deficits such as hemiparesis, aphasia or ataxia might be the second most
common clinical manifestation.7,23,25 Altered mental status, with confusion, lethargy or
agitation, may be the next most common manifestation.11,23,25 Fever was part of the classic
triad of clinical manifestations of brain abscess (headache, focal neurological deficit, and
fever), but this triad is increasingly uncommon and now present in less than 20% of
patients.11,23 The range of reported frequency of fever as a manifestation of brain abscess is
particularly broad, but it is probably less common than focal deficits or altered mental status.
Nausea and vomiting can occur in association with increased intracranial pressure. The new
onset of seizures can be a clinical manifestation of brain abscess.

Table 1

Signs and symptoms of brain abscess

Clinical manifestation Range of frequency

Headache 50–90%
Focal neurological deficit 30–80%
Altered mental status 35–70%
Fever 15–85%

Nausea and vomiting 25–50%

Seizures 5–45%
The most likely pathogens in a brain abscess vary with the anatomic source of infection, as
does the most likely site of the abscess within the brain. As shown in Table 2, brain abscesses
often start with contiguous spread from a paranasal sinus into the frontal lobe and the most
likely pathogen is a member of the Streptococcus milleri group, which includes
Streptococcus anginosus, Streptococcus constellatus and Streptococcus intermedius.10
Among these streptococci, Streptococcus intermedius has emerged as the most frequent
pathogen in brain abscesses.12,13 An odontogenic source of infection leading to brain abscess
is increasingly recognized.11 Odontogenic brain abscesses are most often polymicrobial,
including oral anaerobes such as Fusobacterium nucleatum.14,15 Otogenic brain abscesses
from otitis or mastoiditis are most often in the adjacent temporal lobe and most often with
the same pathogens as those from sinusitis. Hematogenous brain abscesses from
endocarditis, neurosurgery or trauma are frequently multiple and Staphylococcus aureus is a
leading pathogen in this context.10,23,25

Table 2

Most likely pathogens and locations of brain abscess

Anatomic source Most likely pathogen Most likely location

Paranasal sinus Streptococcus intermedius Frontal lobe

Oral cavity Polymicrobial Frontal lobe

Ear Streptococcus intermedius Temporal lobe

Bloodstream Staphylococcus aureus Multiple lobes

What is the management of a brain abscess?

Management of a brain abscess generally includes both antibiotic therapy and

neurosurgery.7,25 The antibiotics should cover the pathogens, but must also be ones able to
cross the blood-brain barrier. If a brain lesion is identified as an abscess, empiric intravenous
antibiotic therapy is begun, often with ceftriaxone or cefotaxime combined with
metronidazole.26 Third generation cephalosporins such as ceftriaxone cover the most
common streptococcal, staphylococcal and other bacterial pathogens in brain abscesses. So,
for instance, in a study of 47 brain abscess cases, all 29 streptococcal pathogens, both
staphylococcal pathogens, and all but 5 other pathogens were sensitive to ceftriaxone; the
only pathogens not covered by ceftriaxone were 3 Pseudomonas aeruginosa and 2 Listeria
monocytogenes.12 Metronidazole covers the oral flora anaerobic bacteria that are sometimes
among the pathogens in brain abscesses.12,26 Neurosurgery is required for the identification
of the causative pathogen, and sometimes drainage to reduce the size of the abscess. With
stereotactic neurosurgical techniques, almost any brain abscess 1 cm or larger is amenable to
stereotactic aspiration.7 Endoscopy can aid the visualization of drainage, which can be
particularly helpful if an abscess is multiloculated with septated compartments.27

What is the prognosis for a patient with a brain abscess?

The prognosis for a patient with a brain abscess has improved. Mortality has declined from
40% in 1960 to 15% in the recent past.7 If a brain abscess is promptly identified and treated,
the majority of patients have a good outcome. Currently, about 70% of patients recover with
minimal or no neurological sequelae.7 The prognosis may not be as good in some groups of
patients. In a recent series of 247 patients from 2009 to 2020, only 43% recovered without
neurological deficits, but 35% of these patients had a malignancy, 35% were
immunocompromised, 33% had head and neck surgery or traumatic brain injury, and 24%
had diabetes mellitus; only 8% died.25 Prompt diagnosis and combined medical-surgical
therapy are the keys to a good outcome.

Teaching points

• The most common causes of new onset seizures vary by age: fever in children,
cerebrovascular disease in older adults, and trauma, tumors, drugs, autoimmunity and
infections in young adults.
• The most common causes of a ring-enhancing lesion in the brain can be sorted into 5
groups: metastases, abscesses, glioblastomas, infarcts (or inflammation) and contusions,
using the first letter of each group to create an acronym MAGIC as a memory aid.
• Most brain abscesses are due to bacteria, often from the normal oral flora, and many brain
abscesses are polymicrobial, including both aerobes and anaerobes.
• Aspirate of the liquid center of a brain abscess is usually the best sample for the clinical
microbiology laboratory to identify the pathogens causing a brain abscess.
• Gram stain, aerobic and anaerobic cultures are generally the most essential testing of the
aspirate of a brain abscess, although it is better to err on the side of ordering too much
rather than too little because aspiration of a brain abscess is a difficult and risk-laden
procedure.
• Management of a brain abscess generally includes both neurosurgery and antibiotic
therapy, with antibiotics that not only cover the pathogens, but also cross the blood-brain
barrier.
• If a brain abscess is promptly identified and treated, the majority of patients have a good
outcome, with no or minimal neurologic sequelae.

Funding
The article processing fee for this article was funded by an Open Access Award given by the
Society of ‘67, which supports the mission of the Association of Pathology Chairs to produce
the next generation of outstanding investigators and educational scholars in the field of
pathology. This award helps to promote the publication of high-quality original scholarship
in Academic Pathology by authors at an early stage of academic development.

References

1. Knollmann-Ritschel B.E.C., Regula D.P., Borowitz M.J., Conran R., Prystowsky M.B. Pathology competencies
for medical education and educational cases. Acad Pathol. 2017;4 doi: 10.1177/2374289517715040. [PMC free
article] [PubMed] [CrossRef] [Google Scholar]

2. Ropper A.H., Samuels M.A., Prasad S., Klein J. eleventh ed. McGraw Hill; New York, NY: 2019. Adams and
Victor's Principles of Neurology; pp. 352–357. [Google Scholar]

3. Smith D.K., Sadler K.P., Benedum M. Febrile seizures: risks, evaluation, and prognosis. Am Fam Physician.
2019;99(7):445–450. [PubMed] [Google Scholar]

4. Yeshokumar A.K., Coughlin A., Fastman J., et al. Seizures in autoimmune encephalitis-A systematic review and
quantitative synthesis. Epilepsia. 2021;62(2):397–407. doi: 10.1111/epi.16807. [PubMed] [CrossRef] [Google
Scholar]

5. Cortese I., Nath A. Case 11: a young woman with ring-enhancing brain lesions. MedGenMed. 2006;8(1):3.
[PMC free article] [PubMed] [Google Scholar]

6. Ropper A.H., Samuels M.A., Prasad S., Klein J. eleventh ed. McGraw Hill; New York, NY: 2019. Adams and
Victor's Principles of Neurology; p. 661. [Google Scholar]

7. Brouwer M.C., Tunkel A.R., McKhann G.M., 2nd, van de Beek D. Brain abscess. N Engl J Med.
2014;371(5):447–456. doi: 10.1056/NEJMra1301635. [PubMed] [CrossRef] [Google Scholar]

8. Alves A.F.F., Miranda J.R.A., Reis F., et al. Inflammatory lesions and brain tumors: is it possible to differentiate
them based on texture features in magnetic resonance imaging? J Venom Anim Toxins Incl Trop Dis. 2020;26
doi: 10.1590/1678-9199-JVATITD-2020-0011. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

9. Zeng T., Xu Z., Yan J. The value of asphericity derived from T1-weighted MR in differentiating
intraparenchymal ring-enhancing lesions-comparison of glioblastomas and brain abscesses. Neurol Sci.
2021;42(12):5171–5175. doi: 10.1007/s10072-021-05226-x. [PubMed] [CrossRef] [Google Scholar]

10. Brook I. Microbiology and treatment of brain abscess. J Clin Neurosci. 2017;38:8–12.
doi: 10.1016/j.jocn.2016.12.035. [PubMed] [CrossRef] [Google Scholar]

11. Hsu G., Zhang J., Selvi F., Shady N., August M. Do brain abscesses have a higher incidence of odontogenic
origin than previously thought? Oral Surg Oral Med Oral Pathol Oral Radiol. 2020;130(1):10–17.
doi: 10.1016/j.oooo.2020.01.008. [PubMed] [CrossRef] [Google Scholar]
12. Darlow C.A., McGlashan N., Kerr R., et al. Microbial aetiology of brain abscess in a UK cohort: prominent
role of Streptococcus intermedius. J Infect. 2020;80(6):623–629. doi: 10.1016/j.jinf.2020.03.011. [PMC free
article] [PubMed] [CrossRef] [Google Scholar]

13. Issa E., Salloum T., Tokajian S. From normal flora to brain abscesses: a review of Streptococcus intermedius.
Front Microbiol. 2020;11:826. doi: 10.3389/fmicb.2020.00826. [PMC free article] [PubMed] [CrossRef] [Google
Scholar]

14. Denes E., Barraud O. Fusobacterium nucleatum infections: clinical spectrum and bacteriological features of 78
cases. Infection. 2016;44(4):475–481. doi: 10.1007/s15010-015-0871-x. [PubMed] [CrossRef] [Google Scholar]

15. Franceschi D., Giuliani V., Giuntini V., Pini Prato G. Brain abscess and periodontal pathogens (Fusobacterium
Nucleatum). Report of a case. Clin Case Rep. 2020;8(12):2488–2493. doi: 10.1002/ccr3.3173. [PMC free article]
[PubMed] [CrossRef] [Google Scholar]

16. Cano E.J., Corsini Campioli C., Rodriguez A.E., Enzler M.J. New-onset seizures and a tangled up Gram's
stain: Actinomyces brain abscess. IDCases. 2020;23 doi: 10.1016/j.idcr.2020.e01024. [PMC free article]
[PubMed] [CrossRef] [Google Scholar]

17. Abo-Zed A., Yassin M., Phan T. A rare case of polymicrobial brain abscess involving Actinomyces. Radiol
Case Rep. 2021;16(5):1123–1126. doi: 10.1016/j.radcr.2021.02.042. [PMC free article] [PubMed] [CrossRef]
[Google Scholar]

18. Robinson C.A. November 2006: a 39-year-old man with new onset seizures. Brain Pathol. 2007;17(2):253–
254. doi: 10.1111/j.1750-3639.2007.00068_2.x. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

19. Corsini Campioli C., Castillo Almeida N.E., O'Horo J.C., et al. Clinical presentation, management, and
outcomes of patients with brain abscess due to nocardia species. Open Forum Infect Dis. 2021;8(4):ofab067.
doi: 10.1093/ofid/ofab067. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

20. Grüter B.E., Reuss A.M., Rushing E.J., Pangalu A., Oertel M.F. An unexpected intracerebral lesion - case
report of a superinfected aspergillosis mimicking a brain metastasis. BMC Infect Dis. 2021;21(1):537.
doi: 10.1186/s12879-021-06176-7. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

21. Mulpur B., Migdady I., Mays M. Clinical and radiographic resolution of multifocal brain abscesses secondary
to Fusobacterium. Neurology. 2020;95(16):749–750. doi: 10.1212/WNL.0000000000010732. [PubMed]
[CrossRef] [Google Scholar]

22. Stebner A., Ensser A., Geißdörfer W., Bozhkov Y., Lang R. Molecular diagnosis of polymicrobial brain
abscesses with 16S-rDNA-based next-generation sequencing. Clin Microbiol Infect. 2021;27(1):76–82.
doi: 10.1016/j.cmi.2020.03.028. [PubMed] [CrossRef] [Google Scholar]

23. Patel K., Clifford D.B. Bacterial brain abscess. Neurohospitalist. 2014;4(4):196–204.
doi: 10.1177/1941874414540684. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

24. Rath T.J., Hughes M., Arabi M., Shah G.V. Imaging of cerebritis, encephalitis, and brain abscess.
Neuroimaging Clin. 2012;22(4):585–607. doi: 10.1016/j.nic.2012.04.002. [PubMed] [CrossRef] [Google Scholar]
25. Corsini Campioli C., Castillo Almeida N.E., O'Horo J.C., et al. Bacterial brain abscess: an outline for diagnosis
and management. Am J Med. 2021;134(10):1210–1217. 10.1016/j.amjmed.2021.05.027 e2. doi: [PubMed]
[Google Scholar]

26. Bodilsen J., Tattevin P., Tong S., Naucler P., Nielsen H. Treatment of community-acquired bacterial brain
abscess: a survey among infectious diseases specialists in France, Sweden, Australia, and Denmark. Eur J Clin
Microbiol Infect Dis. 2021;40(2):255–260. doi: 10.1007/s10096-020-04032-1. [PubMed] [CrossRef] [Google
Scholar]

27. Elmallawany M., Ashry A., Alsawy M.F. Endoscopic treatment of brain abscess. Surg Neurol Int. 2021;12:36.
doi: 10.25259/SNI_800_2020. [PMC free article] [PubMed] [CrossRef] [Google Scholar]